Endometritis

ENDOMETRITIS (endometritis). At the end of the 19th century and at the beginning of the current 20th century, all gynecologists attributed numerous and distinctive changes in the mucous membrane of the uterus to inflammation, designating them with the collective name E., and according to the generally accepted classification of Carl Ruge (C. Ruge), three main types were distinguished: interstitial, glandular, and mixed E. During the last 25 years of the 20th century, the doctrine of E. has radically changed in the sense that now inflammatory processes of the uterine mucosa and its functional changes are differentiated. The modern concept of E. is based mainly on the works of Hitschmann and Adler, R. Schroder, Pankow, and others. Hitschmann and Adler in 1907-08 proved the so-called Vienna doctrine that changes in the uterine mucosa, previously considered inflammatory and described under the name of hypertrophic and hyperplastic glandular E., have nothing in common with inflammation, but represent a physiological phenomenon related to the menstrual cycle (see Menstruation). It should be noted that Slavyansky as early as 1888 pointed to the similarity of the picture of the uterine mucosa in acute E. with its changes during menstruation. The special forms of E. described by Slavyansky and other authors—e. decidualis (thickening of the mucosa in the form of decidual cells), e. villosa (development in the mucosa of papillary formations resembling chorionic villi), e. vascularis (proliferation and dilation of blood vessels)—according to modern views do not belong to inflammatory processes, but represent separate phases of premenstrual, pregravidar, and postabortal changes of the mucosa. Thus, at present, only acute interstitial E. is recognized as an inflammatory process. Older gynecologists distinguished many separate types of chronic E. based on histological pictures, such as: e. fungosa, polyposa, interstitialis, glandularis, exfoliativa, s. membranacea, dissecans, atrophicans, senilis, etc., and almost every major author proposed special terminology. Fungoid E. was called solid or patchy thickenings of the mucosa, polypoid E.—growths of it, sitting on a well-expressed stalk. Interstitial E. was characterized by changes in the stroma, typical for inflammation in general, and glandular E.—by the development of the glandular layer similar to the structure of decidua vera. To e. exfoliativa, s. membranacea were attributed those cases where the mucosa was shed in the plane of the spongy layer with subsequent expulsion of the entire mucosa in the form of a sac or of many small pieces. Under the name e. dissecans, Kubasov described in 1883 the separation of the mucosa together with part of the underlying muscular wall of the uterus due to an inflammatory process in the thickness of the latter. E. atrophicans was called a long-lasting chronic E., in which the mucosa turned into connective tissue, and the glands obliterated or partially underwent cystic degeneration. According to the modern doctrine of Hitschmann-Adler and R. Schroder, most of the listed types of chronic E. do not belong to inflammatory processes of the uterine mucosa, but stand in direct dependence on functional disorders of the ovary and other endocrine glands (pituitary, thyroid). These diseases are now referred to as metropathia and adenomyosis uteri interna, and different authors invest these names with different concepts. According to the doctrine of R. Schroder accepted by the majority of modern gynecologists, the main cause of metropathia lies in the delay of ovulation and as a consequence of such delay in the prolonged existence of a mature follicle and in the absence of the corpus luteum. The absence of corpus luteum hormones and prolonged secretion of folliculin leads to enhanced proliferation of the endometrium, expressed in the form of fungoid or polypoid thickening of the uterine mucosa and in changes in its glands, often of a cystic nature. Developing thromboses, infiltration with leukocytes, and hemorrhages lead to necrosis of the mucosa, which is shed during bleeding. The connection of metropathia with dysfunction of other endocrine glands can be seen in the fact that this disease is observed mainly either from the very beginning of sexual maturity in girls constitutionally inadequate (infantile, less often intersexual type), or in elderly women in the period of extinction of sexual function, in other words, in subjects with impaired correlation of the endocrine system. In the genesis of adenomyosis of the uterus, manifested in the diffuse growth of the glandular layer, according to Albrecht, hormonal and dysplastic factors play the main role. Adenomyosis of the uterus occurs in the climacteric period with the reverse development of the sexual sphere. Both metropathia and adenomyosis of the uterus cause severe and persistent bleeding of the type of meno- and metrorrhagia, leading to severe anemia, sometimes threatening the life of the patient. According to R. Schroder, the anemia in metropathia is caused not only by significant bleeding but also by the disturbance of blood-forming activity of the bone marrow due to the toxic effect of folliculin. In the described bleedings, the differential diagnosis is made between metropathia and adenomyosis of the uterus, on the one hand, and on the other between them and climacteric bleeding, cancer of the body of the uterus, submucous myoma, and polyp; while in a woman of childbearing age, the question arises about the possibility of incomplete abortion or ectopic pregnancy. Exact data for recognizing metropathia and adenomyosis are obtained by microscopic examination of the scraping of the uterine mucosa, revealing characteristic changes in the mucosa and glands. The types of chronic E. described above by older authors were united according to the main clinical sign—bleeding—under the name e. haemorrhagica, and the cause of bleeding was considered inflammation of the uterine mucosa. Therefore, the task of previous therapy was reduced to the destruction and removal of the inflamed endometrium by active intrauterine measures, namely curettage, chemical cauterizations, in particular the widely used injections of tincture of iodine according to Grammaticati, vaporization according to Snegiryev and Pincus, galvanocaustics, etc. The modern doctrine of Hitschmann-Adler, R. Schroder, and Pankow on metropathia and adenomyosis of the uterus sees the cause of these bleedings in primary disorders of the ovarian cycle, which secondarily cause changes in the uterine mucosa, which in the old doctrine on female diseases were called fungoid, polypoid, glandular, exfoliative E. Therefore, a more rational therapy appears to be one acting on the ovarian dysfunction as the main cause of bleeding. Such is organotherapy (corpus luteum preparations according to Adler) in metropathia in young women and castration by X-rays in elderly women, and as a last measure, removal of the uterus. In adenomyosis of the uterus, X-ray castration and removal of the uterus are also indicated. However, it must be pointed out that although the doctrine of the essence of metropathia and adenomyosis of the uterus is accepted by the majority of modern gynecologists, many of them continue to fight bleeding by curettage and various chemical and thermal cauterizations of the uterine mucosa (in particular intrauterous injections according to Grammaticati), despite all the groundlessness, despite the unstable, short-term effectiveness of such intrauterine therapy. In addition, to fight bleeding, irradiation of the spleen (Stefan, Hirsch, and others), liver (Borak and others), and pituitary (Hofbauer) was proposed, but according to Adler, this method is theoretically insufficiently substantiated and the results of its application are few. Significantly better results are given by pituitary preparations, proteinotherapy and injections of gelatin serum act less effectively. In addition to the types of chronic E. listed above, older authors also included e. dysmenorrhoica and dolorosa (Snegiryev) among them, but according to modern doctrine, these diseases have nothing in common with inflammation of the uterine mucosa, but are caused, the first—by ovarian dysfunction, and the second—by inflammation of the lumbar nerves, and therefore should be excluded from the section on E. Inflammatory diseases of the uterine mucosa are distinguished according to the etiology of inflammation, according to the microbes-causative agents, and according to their phases (acute, subacute, and chronic), and practically they break down into gynecological and obstetric E. Since the inflammatory process always takes place in the stroma, there exists only the interstitial form of acute and chronic E., characterized by humoral-cellular exudate of various degrees. Acute gynecological E. is caused by two main factors: 1) traumatic effects on the uterine mucosa and 2) microbes. Traumatic acute E. develops as a result of mechanical, chemical, and thermal irritations and injuries to the mucosa, mainly during therapeutic intrauterine manipulations—during dilation of the cervix with laminaria, during thermal and chemical cauterizations, vaporization, introduction of radium into the uterus, etc. Infectious E. is caused either by the direct penetration of microbes into the uterus or by metastatic carriage of them in general acute and chronic infectious diseases.

Direct entry of microbes into the uterine cavity occurs either as a result of spontaneous ascending infection from the lower part of the genital canal or as a result of mechanical introduction during various instrumental and digital manipulations performed without observing the rules of asepsis and antisepsis. The uterine cavity is generally sufficiently protected against spontaneous penetration of infection by the bactericidal properties of normal vaginal secretions and the mucous plug in the cervix. The uterine cavity is most vulnerable during the period of epithelial desquamation—during menstruation. In addition to infection and intrauterine trauma, acute E. in some cases can be caused by increased blood flow to the pelvic organs during sexual excesses, masturbation, and excessive indulgence in sports. The effect of acute E. on menstruation depends on the severity of the inflammation and on the phase of the menstrual cycle in which the disease occurred. In general, the rule is maintained that menstruation is subject to the influence of the ovary, while the endometrium changes secondarily as a result of primary disorders of the ovarian cycle. Clinically, acute E. manifests as poor general health, pain in the lower abdomen, and sometimes an increase in temperature, but mainly as abundant purulent or bloody-purulent discharge. If infection occurs during menstruation, menorrhagia or a single atypical bleeding of moderate intensity may develop. However, such bleeding has nothing in common with the e. haemorrhagica described by older authors, which is caused by disorders of ovarian function. All the symptoms mentioned are not pathognomonic for acute E. and can be caused by other factors (cancer or erosions of the cervix, ovarian dysfunction, and accidental febrile diseases). Acute E. is most often purulent (e. purulenta) and is caused by infection. In it, small ulcers sometimes form in the superficial layers of the epithelium. If the purulent decay of tissues spreads more extensively over the surface and into the thickness of the mucosa, then larger pieces of necrotic mucosa are shed off. This form is called e. diphtherica or more correctly pseudo-membranacea and is observed in severe infection, mainly after strong cauterizations, douching of the uterine cavity with sublimate, vaporization, and intrauterine application of radium. Among the microbes causing acute E., in terms of frequency of direct infection, gonococci (see Gonorrhea) are in first place, followed by strepto-, staphylococci, and other pathogenic microbes from the vaginal flora (septic E.). Metastatic infection of the endometrium is observed in influenza, pneumonia, scarlet fever, measles, cholera, typhus, and smallpox. Tubercular E. occurs either in the form of typical miliary tuberculosis of the mucous membranes or in the form of caseous degeneration and destruction of the mucosa. The prognosis for acute gynecological E. is generally favorable, as there is a strong tendency to self-healing due to the physiological property of the uterine mucosa to regenerate periodically during menstruation. The main danger of acute E. is that it can serve as a source for further spread of infection to the myometrium and tubes, and with highly aggressive microbes, lead to general infection. Prevention of acute gynecological E. comes down to the prevention of colpitis and endocervicitis, to observing asepsis during intrauterine therapeutic manipulations, and to abstaining from them during menstruation, especially during the period of epithelial desquamation. Treatment of acute E. is strictly conservative and consists of bed rest, application of ice to the abdomen, and in case of pain, suppositories with belladonna or pantopon. Protein therapy does not give clear results. (Specific treatment for gonococcal E.—see Gonorrhea.) Chronic gynecological E. anatomically represents an interstitial inflammation of microbial origin, characterized by the presence of plasma cells of Waldeyer, especially numerous in gonorrhea. In severe cases, the inflammatory process spreads to the basal layer of the mucosa and to the myometrium and even involves the tubes. Thus, E. passes into metroendometritis. The transition of acute E. to subacute and chronic is observed either with reinfection (mainly with gonococci) or with prolonged irritation of the mucosa caused by foreign bodies in the uterine cavity (intrauterine condoms, fragments of laminaria, etc.), as well as submucous myomas, polyps, cancer of the cervix and body, remnants of deciduous tissue, and, according to Driessen, large areas of mucosa not shed during menstruation. In this case, secondary ascending infection usually occurs, which is facilitated by the presence of necrotic tissues in the uterus. With polyps and tumors, infection concentrates in their vicinity and exacerbates with each menstruation. According to the teaching of Adler and Gichman, chronic E. does not cause bleeding, nor does it cause pain between menstruations (Mittelschmerz). The only clinical symptom of chronic E. is purulent leucorrhea, which was previously not paid attention to. However, leucorrhea is not always observed, and mucous and serous discharges are typical for inflammation of the cervix, but not for the body of the uterus. A special form of chronic E. is pyometra, characterized by the accumulation and retention of uterine secretion in the uterine cavity due to scar narrowing or stenosis of the cervical canal. In this disease, various microbes are found in the uterine secretion, mainly strepto- and staphylococci, and the uterine mucosa macroscopically resembles a pyogenic film in the cavity of an abscess (e. atrophicans in old terminology). Pyometra (see Pyometra) usually occurs in elderly women and clinically manifests as periodic discharge of abundant pus, and in some cases, pulling pains in the lower abdomen and fever. Since chronic E. generally has no characteristic symptoms, its diagnosis is established only by excluding other diseases of the uterus and by the etiology of the inflammation of the mucosa. According to modern views, it cannot be considered rational to recommend vaporization of the uterine cavity for diagnostic purposes, as this manipulation is associated with severe trauma to the uterus and can exacerbate the inflammatory process, as well as introduce a new infection from the vaginal flora. In general, chronic E. occurs far less frequently than older gynecologists assumed. The prognosis for chronic E. is favorable for both the patient's life and the local process, which shows a tendency to heal, with the exception of pyometra. The effect of chronic E. on infertility, habitual miscarriage, and on the development of anomalies of the placenta (placenta praevia, marginata, accreta, etc.), as well as on the formation of hydatidiform mole cannot be precisely established and is admitted only with severe changes in the mucosa. Since, according to modern teaching, chronic E. is not a cause of menorrhagia and metrorrhagia, local treatment of the uterine mucosa aimed at stopping bleeding must be considered useless and even harmful. To combat leucorrhea in chronic E., old gynecology recommended intensive disinfection of the uterine cavity by douching with various disinfectant solutions, applications, and cauterizations. Despite the low effectiveness of such treatment, many modern gynecologists continue to use active intrauterine treatment, not taking into account the fact that the cyclic regeneration of the uterine mucosa contains a tendency to self-healing. Rational therapy for chronic E. should be conservative and fight mainly against the primary causes causing and maintaining chronic E., i.e., against polyps, myomas, and cancer, against reinfection, and should also consist in abstaining from active intrauterine manipulations that damage the mucosa and prevent its spontaneous regeneration. An exception to this rule is pyometra, in which dilation of the cervix is indicated to restore outflow from the uterine cavity. In cases where it is not possible to eliminate the stenosis of the cervix, complete removal of the uterus is recommended during the afebrile period. An intermediate position between gynecological and obstetric E. is occupied by post-abortion E. without obvious signs of infection. It is characterized by insufficient regeneration of the mucosa, remnants of gravid decidua, and retention of fetal elements (chorionic villi and syncytial cells). Clinically, post-abortion E. manifests as metrorrhagia, less often in the form of menorrhagia. The cause of bleeding, in the opinion of most gynecologists, lies in necrosis and thrombosis of the mucosa. The bleeding can turn into more or less abundant brownish discharges. Treatment consists in scraping the uterine mucosa and in prescribing ergot or styptisin preparations for better contraction of the uterus. Obstetric E. can develop during pregnancy, as well as during and after childbirth and miscarriages.

Endometritis of pregnancy arises on the basis of chronic gynecological endometritis and is characterized by the lush development of the decidua with numerous dilated capillaries and small vessels. This vascular network easily ruptures when blood pressure rises and causes frequent, but moderate, bleeding, which usually does not affect the condition of the pregnant woman or the nutrition of the fetus, and only in rare cases, due to significant hemorrhage into the fetal membranes, miscarriage occurs. In this case, the ovum has a distinctive appearance due to the spotted whitish-yellow coloring and uneven thickening of the decidual masses—so-called endometritis decidua polyposa, s. toberosa. The usual form of endometritis of pregnancy is called endometritis decidua haemorrhagica and is observed mainly in the first months of pregnancy, while in the second half of pregnancy this anomaly of the decidua gradually disappears due to its stretching and emptying of the vessels caused by the enhanced growth of the ovum. Only in exceptional cases does the bleeding continue until the end of pregnancy, and the thickened lobules of the decidua are shed along with the placenta or later in the postpartum period, and sometimes force the physician to resort to curettage to stop severe bleeding. Treatment for hemorrhagic endometritis of pregnancy consists of prolonged bed rest until bleeding stops and the elimination of all conditions that increase blood pressure. Older authors also described a special form of endometritis of pregnancy—decidual hydorrhea (hydroroea gravidarum), the clinical symptom of which was the periodic discharge of fluid that had accumulated between decidua vera and reflexa due to inflammatory hypersecretion. At present, this form of endometritis is denied, while the discharge of fluid during pregnancy is explained by the partial escape of amniotic fluid due to premature rupture of the fetal membranes. The distinctive feature of the described forms of endometritis of pregnancy is that microbes play no role in them; conversely, endometritis during and after childbirth and miscarriages (puerperal) is always of microbial origin. The sources of infection in puerperal endometritis are the same as in acute gynecological endometritis, i.e., infection enters the uterine cavity either exogenously or endogenously—from the vagina—or metastatically. Metastatic infection is observed mainly in acute streptococcal infections—angina, tonsillitis, otitis, influenza, to which parturient women are especially susceptible. Regarding the possibility of endogenous-vaginal infection of the uterine mucosa, the opinions of authors differ. Some of them, headed by Bumm, recognize only the exogenous source of infection, while most modern obstetricians admit in a certain percentage of cases endogenous-vaginal infection, and finally, according to Schottmüller, with the modern organization of hospital obstetrics, exogenous infection is excluded and all puerperal endometritides are caused by microbes of the vaginal flora, penetrating the uterus spontaneously or being introduced mechanically during therapeutic intrauterine manipulations during childbirth and in the postpartum period. According to the generally accepted opinion, spontaneous penetration of microbes into the uterine cavity occurs after the passage of waters, but according to the research of Harris and Brown, microbes can penetrate into the lower segment of the uterus even with an intact fetal bladder. Endometritis during childbirth and miscarriages is clinically characterized by elevated temperature and foul-smelling waters; the actual puerperal endometritis manifests later in the form of fever and signs of infection of the mucosa, however, in some cases it is difficult to draw a clear line between these forms. Puerperal endometritis is the initial phase of infection, which depending on the various relationships between the potential energy of micro- and macroorganisms either remains a local inflammation of the uterine mucosa or serves as the primary focus for the further spread of infection. Puerperal endometritis is usually accompanied by endocervicitis and colpitis, and in it, to a greater extent than in gynecological endometritis, the myometrium is involved in the inflammatory process. Reactive processes in the mucosa and in the thickness of the uterine wall have a hematogenous and histogenous nature and are expressed by enhanced leukocytosis (leukocytic barrier) and the fact that some cells of the mesenchyme and the endothelium of capillaries and vessels become wandering and exhibit phagocytic ability. The main causative agents of puerperal endometritis are aerobic and anaerobic hemolytic and non-hemolytic streptococci, staphylococci, and much more rarely gonococci and other microbes (Bacillus coli, diplococcus of Frenkel, Bacillus perfringens, etc.). In the clinical-bacteriological aspect, two main forms of puerperal endometritis are distinguished—putrid and septic. This division is based on Duncan's teaching about two types of microbes—saprophytes and parasites. Old and modern supporters of Duncan's teaching, for example Bublichenko, Siegwart, Waltgart, and many others, attach great prognostic significance to the difference between putrid and septic endometritis, considering the first a non-dangerous disease and the second more dangerous. However, according to modern data, such a sharp distinction between these two forms of infection has no sufficient basis either in the histological picture of the endo- and myometrium or in the clinical course and prognosis. The absence of a clear difference between the course and outcomes of putrid and septic endometritis is explained by the fact that in infection of the mucosa, the leading role belongs to the reaction of the macroorganism of the patient to the infection, and not to the specific properties of one or another causative agent of inflammation, which play only a subordinate role. Therefore, in some cases, with an insufficient reaction of the macroorganism, both putrid and septic endometritis can develop into a severe form of puerperal disease, and in others, with an effective reaction of the body, both types of microbes (saprophytes and parasites) cause only inflammation of the uterine mucosa. Clinically, the puerperal form of endometritis manifests in the changed character of the lochia and in the delayed involution of the uterus. Discharges from the uterus are usually more abundant and purulent, and when anaerobes are present (Streptococcus putridus of Schottmüller and Bacillus perfringens), a more or less strong putrid odor appears in them. Prolonged and more abundant discharge of bloody secretions in most cases indicates incomplete emptying of the uterus. Due to the greater or lesser involvement of the uterine wall in the inflammatory process, the ability of the uterus to involute is reduced, therefore, in infectious endometritis, a greater or lesser subinvolution of the uterus is always observed. Poor contraction of the uterus leads to the accumulation of discharge in it, which creates favorable conditions for microbes and thereby contributes to the intensification of endometritis and the absorption of infected secretions. Puerperal endometritis is accompanied by a moderate elevation of temperature, which can reach 38-39° when there is retention of discharge in the uterus and sometimes is complicated by chills. Short-term elevations of temperature without clear signs of inflammation of the uterine mucosa, so-called diseases without localization, according to Hamm, should be attributed to mild endometritis, mostly of endogenous-vaginal origin. The course of puerperal endometritis is characterized by a gradual decrease in temperature to normal, improvement in the involution of the uterus, and the appearance of normal lochia. The duration of puerperal endometritis averages 7-10 days. In puerperal endometritis, a much greater danger than in gynecological endometritis is the possibility of further spread of infection, which is due, on the one hand, to the large wound surface and enhanced absorption in the puerperal period, and, on the other hand, to the more weakened reaction of the body of the parturient woman due to birth trauma and the greater or lesser blood loss during childbirth. Puerperal endometritis by itself gives a quite favorable prognosis, as it represents a purely local inflammation, indicating a sufficiently effective reaction of the body and the weak aggressiveness of the infection. The severe form of septic endometritis with a fatal outcome described by many authors should be classified under the heading of severe sepsis, which develops from inflammation of the mucosa due to the very great aggressiveness of microbes and the almost complete absence of the body's reaction to the infection. In such cases, at autopsy, almost no macroscopic changes are found in the organs, except for the phenomena of endometritis and more or less expressed parenchymal degeneration of the myocardium, liver, and kidneys, but from the blood during the life of the patient or at autopsy, it is almost always possible to obtain the microbe, mainly hemolytic streptococcus. Consequently, in such cases, we are dealing with fulminant hematogenous sepsis, and endometritis is only the primary source of it. Prevention of puerperal endometritis is entirely included in the preventive measures against puerperal infection in general, especially during childbirth (see Childbirth, Postpartum period). In the therapy of puerperal endometritis, there are two directions—active and conservative.

The active method aims to destroy the infection in the uterine cavity by washing it with various disinfectant solutions, treating it with iodine tincture, introducing gases (oxygen according to Thiriar and Reverden, ether according to Varnecros), and curettage, while always ignoring the possible penetration of microbes into the thickness of the uterine wall and not taking into account the reactive processes in it. Supporters of the conservative method, whose number is constantly increasing, point to the insignificance and short-term effect of the above-mentioned intrauterine manipulations, but above all emphasize the danger of the inevitable trauma to the uterus during these procedures, which destroys the protective barrier and thrombi of the placental site and in the thickness of the myometrium, and thus threatens to cause further spread of infection. At present, the number of opponents of late curettage of the uterus in the absence of remnants of the ovum or placenta in it has particularly increased. Supporters of the conservative method believe that the physician's task in puerperal E. consists in localizing the infection within the uterine cavity and in stimulating the body's reaction. The first task can only be achieved indirectly, namely by avoiding any trauma to the uterus and supporting the tone of its musculature. Therefore, bed rest for the patient, application of ice to the abdomen, and administration of ergot or pituitrin preparations are recommended. The conservative school considers measures to artificially enhance the outflow of uterine secretions (introduction of tampons, drains, constant irrigation according to Morozov-Snegirev) to be unnecessary, since in puerperal E. the discharge of lochia is sufficiently ensured by the dilation of the cervical canal; exceptions are cases of sharp flexion of the uterus forward or backward, which require its artificial correction by bimanual maneuvers. In the absence of such flexions of the uterus and in case of retention of lochia in it, the Fowler position (inclined position of the bed with the head end elevated), recommended by English and American authors, gives good results. With the described therapy, vaginal douches are unnecessary in the vast majority of cases and can be used only as a hygienic measure in cases of very abundant and foul-smelling discharge. Stimulation of the body's general reaction is best achieved by autogenous blood therapy. When signs of infection spreading beyond the uterus appear, the focus of treatment shifts to combating these complications, and the therapy of puerperal E. moves to the background. The most radical treatment for puerperal E.—excision of the uterus as the primary focus of infection—has few supporters, since removal of such an important organ is completely irrational for simple puerperal E., which has a very favorable prognosis. (Regarding infectious E. in incomplete emptying of the uterus after miscarriages and births—see the Puerperium, postpartum hemorrhages.)

€. Sazonov. ENDOMIXIS (from Greek endo-internal and myxis-mixing), a special type of sexual process in infusoria, described by Woodruff and Erdman (1914). It is observed either in freely motile (paramecium) or in encysted stages of infusoria. During E., the macronucleus is destroyed and dissolved, while the micronucleus divides, and from the products of its division a new nuclear apparatus is restored. E. corresponds to parthenogenesis, as R. Hertwig pointed out, and under certain conditions replaces conjugation, periodically repeating after more or less definite intervals.